BACKGROUND Relatively limited epidemiological data are available regarding the prognosis of congestive heart failure (CHF) and temporal changes in survival after its onset in a population-based setting. METHODS AND RESULTS Proportional hazards models were used to evaluate the effects of selected clinical variables on survival after the onset of CHF among 652 members of the Framingham Heart Study (51% men; mean age, 70.0 +/- 10.8 years) who developed CHF between 1948 and 1988. Subjects were older at the diagnosis of heart failure in the later decades of this study (mean age at heart failure diagnosis, 57.3 +/- 7.6 years in the 1950s, 65.9 +/- 7.9 years in the 1960s, 71.6 +/- 9.4 years in the 1970s, and 76.4 +/- 10.0 years in the 1980s; p < 0.001). Median survival after the onset of heart failure was 1.7 years in men and 3.2 years in women. Overall, 1-year and 5-year survival rates were 57% and 25% in men and 64% and 38% in women, respectively. Survival was better in women than in men (age-adjusted hazards ratio for mortality, 0.64; 95% CI, 0.54-0.77). Mortality increased with advancing age in both sexes (hazards ratio for men, 1.27 per decade of age; 95% CI, 1.09-1.47; hazards ratio for women, 1.61 per decade of age; 95% CI, 1.37-1.90). Adjusting for age, there was no significant temporal change in the prognosis of CHF during the 40 years of observation (hazards ratio for men for mortality, 1.08 per calendar decade; 95% CI, 0.92-1.27; hazards ratio for women for mortality, 1.02 per calendar decade; 95% CI, 0.83-1.26). CONCLUSIONS CHF remains highly lethal, with better prognosis in women and in younger individuals. Advances in the treatment of hypertension, myocardial ischemia, and valvular heart disease during the four decades of observation did not translate into appreciable improvements in overall survival after the onset of CHF in this large, unselected population.

Survival after the onset of congestive heart failure in Framingham Heart Study subjects.

BACKGROUNDAtrial fibrillation is common in advanced heart failure, but its prognostic significance is controversialMETHODS AND RESULTSWe evaluated the relation of atrial rhythm to overall survival and sudden death in 390 consecutive advanced heart failure patients Etiology of heart failure was coronary artery disease in 177 patients (45%) and nonischemic cardiomyopathy or valvular heart disease in 213 patients (55%) Mean left ventricular ejection fraction was 019 +/- 007 Seventy-five patients (19%) had paroxysmal (26 patients) or chronic (49 patients) atrial fibrillation Compared with patients with sinus rhythm, patients with atrial fibrillation did not differ in etiology of heart failure, mean pulmonary capillary wedge pressure on therapy, or embolic events but were more likely to be receiving warfarin and antiarrhythmic drugs and had a slightly higher left ventricular ejection fraction After a mean follow-up of 236 +/- 303 days, 98 patients died: 56 (57%) died suddenly, and 36 (37%) died of prog

Prognostic significance of atrial fibrillation in advanced heart failure. A study of 390 patients.

Hemodynamically significant primary anomalies of the coronary arteries are those which alter myocardial perfusion. There are four major types: coronary artery fistulae, origin of the left coronary artery from the pulmonary artery, congenital coronary stenosis or atresia, and origin of the left coronary artery from the right sinus of Valsalva, with subsequent passage of the vessel between the aorta and right ventricular infundibulum. The angiographic features of these lesions are discussed.

Hemodynamically significant primary anomalies of the coronary arteries. Angiographic aspects.

Certain clinical and cardiac necropsy findings are described in 152 patients aged 16 to 78 years (mean 45) with idiopathic dilated cardiomyopathy: 109 (72%) were men and 43 (28%) were women. Compared with the women, the men had a significantly (p less than 0.05) shorter mean duration of chronic congestive heart failure (CHF) (43 vs 69 months), a higher percentage of habitual alcoholism (40 vs 24%) and a higher mean heart weight (632 vs 551 g). The male to female ratio among the 58 known alcoholics was 7.3:1 and among the 70 known nonalcoholics, 1.5:1 (p less than 0.05). The mean duration of clinical evidence of CHF was similar among the known alcoholics and the known non-alcoholics (each 50 months). Of the 152 patients, 148 (97%) had clinical evidence of chronic CHF; in 114 patients it was the initial manifestation of idiopathic dilated cardiomyopathy, and in most it became intractable and caused death. The interval from onset of chronic CHF to death (known in 120 patients) ranged from 1 to 264 months (mean 54). Comparison of the 27 patients surviving greater than 72 months after onset of chronic CHF to the 64 patients surviving less than or equal to 36 months disclosed a significantly higher frequency in the longer survival group of older patients, of women, of habitual alcoholics, of patients with chest pain syndromes, diabetes mellitus, pulmonary emboli, of patients treated with warfarin and of patients with larger hearts at necropsy. Each of the 4 patients without chronic CHF died suddenly and sudden death was the initial manifestation of idiopathic dilated cardiomyopathy in them. An additional 33 patients also died suddenly, but each of them previously had had chronic CHF. Of the 79 patients (of the 131 for whom information was available) with either pulmonary or systemic emboli or both, 67 (85%) had either right- or left-sided thrombi or mural endocardial plaques or both, whereas of the 52 patients without emboli, 36 (69%) had intracardiac thrombi or plaques (p less than (0.05). Electrocardiograms in the last 6 months of life in 101 patients disclosed atrial fibrillation in 25; complete left (41 patients) or right (6 patients) bundle branch block or indeterminate intraventricular conduction delay (4 patients) in 51 patients; QRS voltage indicative of ventricular hypertrophy in 44 patients (left ventricular in 39 patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Idiopathic dilated Cardiomyopathy: Analysis of 152 necropsy patients

Sudden unexpected deaths have been reported with antipsychotic use since the early 1960s. In some cases the antipsychotic may be unrelated to death, but in others it appears to be a causal factor. Antipsychotics can cause sudden death by several mechanisms, but particular interest has centred on torsade de pointes (TdP), a polymorphic ventricular arrhythmia that can progress to ventricular fibrillation and sudden death. The QTc interval is a heart rate-corrected value that represents the time between the onset of electrical depolarisation of the ventricles and the end of repolarisation. Prolongation of the QTc interval is a surrogate marker for the ability of a drug to cause TdP. In individual patients an absolute QTc interval of >500 msec or an increase of 60 msec from baseline is regarded as indicating an increased risk of TdP. However, TdP can occur with lower QTc values or changes.

Antipsychotic-Related QTc Prolongation, Torsade de Pointes and Sudden Death

Clinical studies on the cardiac performance by means of transseptal left heart catheterization. II. Left ventricular function in high output heart diseases, especially in hyperthyroidism.

The incidence of cardiac abnormalities was studied in 107 cases with chronic alcoholism, admitted to a psychiatric ward. More than half of them adhered to drink Japanese sake almost exclusively.Either palpitation or shortness of breath was seen in 49 cases, cardiothoracic ratio was more than 0.50 in 15 of the 78 cases examined, and abnormal ECG was obtained in 65 of the 103 cases.Among ECG abnormalities, broad and tall PII, high RV5, high T in leads V2 and V3 and QT prolongation were the most frequent. Various arrhythmias and conduction disturbances were also seen.The clinical picture suggested more than incidental association of diffuse myocardial involvement with chronic alcoholism.

Cardiac abnormalities in chronic alcoholism. An evidence suggesting association of myocardial abnormality with chronic alcoholism in 107 Japanese patients admitted to a psychiatric ward.

The role of heavy drinking as a cause of cardiac abnormality was studied in 436 male registrates to a health assessment program for actively working adult people. This group of subjects as a whole was also taken as a sample of nonhospital population, and the incidence of heavy drinker in it was compared to that in 47 male patients with nonobstructive primary cardiomyopathy seen in a cardiology clinic.In the 246 uncomplicated "health assessment" registrates, daily drinking of more than 125ml of ethanol was associated with a significantly increased incidence of cardiomegaly. Moderate drinking (75 to 125ml of ethanol) was associated with a high incidence of sinus tachycardia and premature contractions, but not with cardiomegaly. Daily drinking, even in less amount, was apparently significant as a cofactor causing cardiomegaly, when associated with hypertension.The incidence of heavy drinker was significantly higher in cases with, than in cases without, cardiomegaly among the uncomplicated "health assessment" registrates. It was also higher in male patients with primary nonobstructive cardiomyopathy than in the total nonhospital population.From these and previously collected data, a drinking habit equal to, or more than 125ml of ethanol daily, for 10 years or longer, was suggested as a criterion for diagnosis of clinically significant alcoholic cardiomyopathy.Specific association of chronic hypertension or atherosclerotic vascular disease with heavy drinking was not shown, and the mechanism by which ethanol induces the cardiomyopathy was not made clear.

The Incidence of Myocardial Abnormalities in Man Related to the Level of Ethanol Consumption A Proposal of a Diagnostic Criterion of Alcoholic Cardiomyopathy

Etiology of QT prolongation and T wave high voltage was studied in 90 chronic alcoholics in relation to history of alcoholism, blood chemical values, heart rate and QRS voltage with a technic of multiple regression analysis. Incidences of QT prolongation (22%), T wave high voltage in lead V2 (9%), hypopotassemia (23%), hypocalcemia (26%) and hypomagnesemia (28%) were high, despite these examinations were done after relatively long abstention period (35 days on average). Sinus tachycardia (19%) and QRS high voltage (SV1 + RV5 exceeding 4 mV, 41%) were also frequent. Unexpectedly, QT interval did not correlate to serum electrolytes, including calcium. Major factors associated with QT prolongation were sinus tachycardia, longer abstention period and larger amount of daily alcohol consumption. Although the reason of each association was not quite clear, alcoholic myocardial damage may be a cause of QT prolongation. Voltage of T wave in lead V2 was sensitive to serum potassium level, but the observed tendency of hypopotassemia acted to the direction against high voltage of T wave. The sole factor positively associated with high voltage of TV2 was high QRS voltage, which may be a manifestation of left ventricular hypertrophy.

Etiology of QT Prolongation and T Wave Changes in Chronic Alcoholism

The regional contraction sequence of the left ventricle (LV) was analyzed by 16mm. cineangiocardiograms (in LAO, 40 frames per sec.) of 5 control subjects, 4 patients with mitral insufficiency, 2 with idiopathic hypertrophic subaortic stenosis (IHSS), 2 with idiopathic myocardial hypertrophy and 3 of myocardial disease with LV dilatation.The LV cavity was divided into basal, middle and apical portion, and internal width (diameter) for each portion was measured on a line drawn perpendicular to the long axis at 3 equally spaced points. The time course of the length of the diameters in percentage of the initial length was compared, and circumferential shortening velocity (Vcs) and total extent of circumferential shortening were calculated for each diameter. Regional contraction sequence was also analyzed by superimpositon of serial LV silhouettes during systole.In control subjects, a synchronized contraction sequence was suggested, and regional circumferential shortening velocity was inversely related to the initial length of corresponding diameter. In hypertrophied and dilated hearts of mitral insufficiency or in IHSS, an earlier onset and/or more rapid contraction of the basal portion were noted. The possible relationship between asynchronism of the contraction sequence and alterations of ventricular geometry and of myocardial architecture of the LV were discussed. In myocardial disease with dilated LV, both shortening velocity and extent of shortening were markedly reduced.The method described here allows direct observation of the pattern of regional contraction sequence and also gives clinical indices of contractile state of the myocardium in normal and diseased LV in man.

A cineangiocardiographic study of the regional contraction sequence of the normal and diseased left ventricle in man.

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